How To Arrest Sudden Cardiac Death

 

Sudden cardiac death (or sudden cardiac arrest) is a common, deadly problem and is often the first manifestation of heart disease. It is an abnormal heart rhythm most often caused by ventricular fibrillation (an irregular heart rhythm from the lower chambers of the heart).  When the heart’s ventricles are fibrillating, they cannot pump blood to the brain and vital organs. If not treated promptly, this leads to death.  Sudden cardiac arrest affects 350,00 people in the US each year. Less than 20% of sudden cardiac arrest victims have their rhythm restored to normal and only 10% survive to leave the hospital, which means the death rate is 90%.

 

The cause of sudden cardiac arrest depends on the age of the victim and the type of underlying heart disease.  In patients over the age of 35, the overwhelming cause of sudden cardiac arrest is a heart attack. A heart attack occurs when a plaque or blockage in a heart artery breaks open and a blood clot is formed stopping the blood flow to the heart muscle. It is important to realize that a heart attack and sudden cardiac arrest are not the same thing. A heart attack is one of the causes of sudden cardiac arrest and primarily a plumbing problem (the artery and the blood flow) while sudden cardiac arrest is an electrical problem (an abnormal rhythm). In those under age 35 sudden cardiac arrest is usually caused by a congenital heart problem. The person is born with an abnormal heart muscle, or an abnormal electrical system, or an abnormal origin of one the heart arteries. 

 

The strategies to prevent sudden cardiac arrest from becoming sudden cardiac death include prompt treatment and primary prevention. Prompt treatment involves recognizing that someone is in cardiac arrest, initiating cardiopulmonary resuscitation (CPR) and performing defibrillation as soon as possible. The American Heart Association recommends hands only CPR (chest compression only, no mouth-to-mouth breathing). The initiation of prompt CPR has been shown to save lives. Definitive treatment of sudden cardiac arrest is defibrillation, an electric shock to the heart that restores the heart to normal rhythm. The shock is usually provided by an Automatic External Defibrillator (AED), a small portable device that is brought to the victim’s side. The sooner the patient is shocked, the greater the chance of surviving. Fifty percent of victims of sudden cardiac arrest survive if shocked within two to three minutes, but only ten percent will live if the shock is more than ten minutes from the time of collapse.  Every minute spent waiting for an AED decreases the odds of survival by 7-10%. Having an AED as close as possible to potential victims is lifesaving.  

 

The biggest barriers to successful resuscitation are getting an AED to the victim as soon as possible and having bystanders deploy the device. Fortunately, AEDs seem to be everywhere. About 500,000 to 1 million were sold in the US last year and there are about 3.2 million AEDs in public settings. AEDs are placed in areas where there are large public gatherings (such as airports, schools, stadiums, sports complexes). AEDs have been successfully deployed by police, firemen, sports trainers, and bystanders. In large public spaces, how close together should AEDs be placed?  The American Heart Association recommends an AED within a 3-to-5 minute round trip walk from anywhere in a public place. This translates to each AED covering about 100 yards in each direction. Aside from large public spaces, where should AEDs placed so bystanders can find and use them? One study from Toronto showed coffee shops and bank ATMs to be the best for coverage. A study from England felt that AEDs near mailboxes was best. A study from Taiwan concluded that bus stops, convenience stores and pharmacies were optimal. All studies emphasized areas where the public would be familiar with the AED location, potentially enhancing the use of AEDs by bystanders. 

 

Unfortunately, only 15% of sudden cardiac arrests take place in a public area. The vast majority (85%) of events take place in a private home. In the private setting, it is estimated that only 6% of sudden cardiac arrest victims might have an AED close enough for use. What is the optimal density of AEDs and how can they be brought to victims in residential areas? Multiple studies have concluded that the optimal density of AEDs is between 5 and 41 AEDs per square mile. Unfortunately, in a country as large as the United States, this density will be difficult to achieve nationwide. To increase AED coverage, especially in remote areas, multiple studies have advocated using drone delivery of AEDs to cardiac arrest patients. One study showed that drone delivery of an AED was 3 minutes faster and beat ambulance arrival in 67% of cases. In a situation where time is critical, drones may make a difference.

 

Unfortunately, even when an AED is available, it may not be used. One recent study reported that even if an AED was one minute walk away from a victim, bystanders only used the device 16% of the time. Fortunately, on December 10 2024, Congress passed the HEARTS Act expanding access to AEDs and increasing training for CPR and AED use. 

 

Primary prevention aims to identify people who may at risk for sudden cardiac arrest before an event occurs. This is especially important since cardiac arrest is often the first manifestation of heart disease in a person. For those over 35 years old, there are no specific recommendations for screening.  General measures to reduce the risk for heart attack are emphasized including following a heart healthy lifestyle (staying active, watching a good diet, not smoking, keeping weight under control, treating high blood pressure and/or high cholesterol). Routine stress testing doesn’t reduce the risk for cardiac mortality, but doing a stress test before starting an exercise program is prudent, especially if there are one or more cardiac risk factors. One way to reduce the risk for sudden cardiac arrest is exercise. One recent study showed that vigorous physical activity of 20 minutes per week reduced the risk for cardiac arrest. Moderate exercise of 360 minutes per week (51 minutes per day) also lowered cardiac arrest risk. 

 

For athletes who are under the age 35, screening is performed. Although cardiac arrest is rare in athletes (1 in 63,00 college athletes have cardiac arrest each year) certain populations are at higher risk. Men have 2 to 10 times the risk as women. Black athletes have 5 times the risk compared to white athletes. Athletes in certain sports (basketball, soccer, cycling and football) are at higher risk. Screening involves a questionnaire asking about symptoms and family history. An electrocardiogram (EKG) is performed on all athletes and a cardiac ultrasound (echocardiogram) is done on those with high risk (for example someone with an abnormal EKG). Many professional athletes (especially football, basketball and soccer players) are screened before a contract is signed.  In addition, Division 1 college athletes are screened. Although screening is controversial, it has been shown that screening prevents sudden cardiac arrest in multiple populations. A recent study reported that sudden cardiac arrest has been steadily declining in college athletes over the past 20 years. 

 

What can the average person do to reduce the risk for sudden cardiac arrest personally and in the community? On a personal level, follow a good heart healthy lifestyle and keep up with the recommended amount of exercise. From the community standpoint, take a CPR class at a local hospital. Most classes teach basic CPR and the proper use of an AED. In addition, take notice of the location of AEDs during your daily activities. You never know when you might use one. 

 

 

How to Fix a Christmas Carol Earworm and Other Healthy Holiday Tips

Everyone has had this experience. You are minding your own business and, all of a sudden, a tune pops into your head. It could be a favorite song or a song you heard on your favorite streaming service. It could be a jingle for a product or a medication. At this time of year, it could be a Christmas carol. The refrain or the catchy lyrics play over and over in your head and you can’t seem to get rid of it. What is this phenomenon?  Why do certain jingles jangle around in the mind?  Why are holiday songs so prone to being stuck in the brain?

 

The experience of having music looping in one’s head is commonly known as an earworm. Other names for the phenomenon are stuck song syndrome, sticky music and musical imagery repetition. The medical term is involuntary musical imagery.  The term earworm was coined in 1979 by a psychiatrist and is derived from the German word ohrwurm, which means musical itch. Earworms mostly appear spontaneously. They can occur when the mind is wandering or daydreaming. They can be associated with exposure to a song, either immediately or, more commonly, many hours later.  An earworm can be triggered by a song that evokes a strong memory or specific situation.  Women are more prone to earworms than men as are those who are musically inclined. The typical loop of music lasts from 20 to 30 seconds and plays back over and over for about 10 to 30 minutes, although rare cases can last for hours. Songs that have faster tempos or long, sustained notes are more likely to stick in the head. 

 

The first known ad jingle was aired in 1926 on a radio station in Minneapolis. The ad was for the cereal Wheaties and each time the jingle was played, it was sung live in the radio studio. The ad (and the jingle) was successful, increasing sales of Wheaties by 60%, possibly by triggering midwestern earworms. The study of earworms far preceded the Wheaties jingle. Earworms have been studied since 1885. However, modern media (radio, television, music streaming) have bombarded us with songs and jingles and have made earworms extremely common. A study of 12,000 people from Finland found that 89% of people experienced an earworm at least once per week. About 20% of participants had an earworm multiple times a day. They also found that earworms decreased with advancing age. The incidence of earworms was confirmed in a study of 240 college students published in 2020. In the study, 97% of participants had an earworm within the past month. 

 

Holiday songs are fertile ground for earworms for multiple reasons. First, there is opportunity. The songs are everywhere at this time of year (on radio, on television, in stores) and played constantly. Holiday songs also evoke strong memories, which in turn can unearth an earworm. The structure of the songs themselves are conducive to promoting earworms. Holiday music by design is simple and singable. The simple structure is easy for the brain to memorize thus laying down tracks in our minds for future playback. Lastly, many holiday songs have a common chordal structure. These chords are pleasant and festive evoking good memories; ripe territory for an earworm.

 

Is that holiday song rattling around the ear canal dangerous? Most of the time, earworms are harmless. In fact, they are part of a healthy brain and help us lay down memories. On the other hand, patients with obsessive compulsive disorder can have earworms under stress and earworms that last for hours and hours can be a sign of depression. If an earworm is accompanied by other symptoms, such as blacking out, confusion, loss of vision or a seizure, then a medical evaluation is indicated. 

 

So, earworms are not usually harmful but they can be annoying. How can we scratch this musical itch?  There are several proven ways to rid oneself of an earworm. One way is to walk at either a faster or slower pace than the tempo of the song. Another way is distraction. Read a book, watch a movie or engage in a task that requires concentration. This will redirect the brain. Speaking of redirecting, try changing your environment; go into a different room or take a walk outside. Another obvious approach is listening to a different song. One less obvious way to get rid of an earworm is to chew gum!

 

Aside from squishing holiday song earworms, what other recommendations can be made for a healthy holiday? Here are eight essential ingredients, loosely modeled after the American Heart Association Life’s Essential Eight:

1.     Diet: try to stick to a heart healthy Mediterranean diet

2.     Diet: try to limit sugary treats and snacks

3.     Diet: when possible while cooking, substitute olive oil for butter 

4.     Exercise: try to maintain your regular exercise program during the holidays

5.     Alcohol: try to limit alcohol. If you are drinking, limit to just one per night

6.     Socialize: with family and friends, as much as possible

7.     Sleep: try to maintain your regular sleep pattern and duration

8.     Weight: try not to gain too much weight at the holidays!

 

Let’s have a safe, healthy and earworm free holiday season!

 

The Presidential Coronary Calcium Score and the Power of Zero

 

“Maybe I’ll win

Saved by zero”

The Fixx, 1983

 

Since the 1990’s, the U.S. Presidents and the Presidential candidates have undergone coronary calcium scores. What can we learn from their results? Let’s look at two examples. Let’s call them the Clintons. Hillary Clinton reportedly had a coronary calcium score of 0. As far as we know, she has not had any heart disease. Bill Clinton’s coronary calcium score was over 1000. He subsequently required open heart bypass surgery. Can you guess the coronary calcium scores of Presidents George Bush, Barack Obama and Donald Trump? What is the coronary calcium score and can you be “saved by zero”?

 

To understand coronary calcium, we must understand the process of atherosclerosis in the heart arteries. In susceptible individuals, plaque formation starts at an early age, the 20’s and 30’s. The initial plaque in the heart arteries is made of cholesterol, what is called “soft” plaque or “fatty” plaque. If we did a CT scan at this stage, no calcium would be detected. Over time, plaque progression continues and by the age of 50 to 60, calcium is deposited in the plaque. The plaque is now considered “hard” plaque. At this stage, a CT scan would detect calcium in the artery. Coronary calcium therefore detects the presence of plaque in the heart arteries. It does not tell us if the plaque is limited to the artery wall or if the plaque is causing significant blockage to the blood flow (obstruction can be determined with a stress test or a heart catheterization).  

 

What is the coronary calcium score and how is it used? Coronary calcium score is obtained with a CT scan. There is no fasting, no preparation, no intravenous and no dye used. The person goes under the CT scanner, holds their breath for about one minute, the scan is taken and done. What do the results mean? For people between the ages of 40 and 75 without established heart artery disease, the score is used as follows. A score greater than 100 represents extensive plaque and an increased risk for future cardiac events (heart attack, blocked heart artery, stroke, cardiac death). In this case a statin (and perhaps aspirin 81 mg once per day) is recommended. A score between 1 and 99 is intermediate. Even a low calcium score (between 1 and 10) is associated with a two times greater risk for cardiac events compared to score of zero. In this population, a statin is recommended if high risk characteristics are present (age over 55, family history of premature heart disease, persistently elevated LDL cholesterol or triglycerides, evidence for inflammation or elevated lipoprotein a in the blood). 

 

What does a coronary calcium score of zero represent? There are two clinical possibilities. One is that there is no heart artery plaque. The other scenario is that there is soft or fatty plaque present, which has not yet calcified. Most studies have found that among patients with coronary calcium of zero, there is a very low likelihood of blockage in the heart arteries and a low risk for heart events (heart attack, stroke, death). However, one study looked at 10,000 people and found that 45% of them had a coronary score of zero. Among those with zero scores, 1.8% still had at least one artery blocked 50% or greater. The prognostic value of a zero score was less for those under the age of 45 (they likely had not had enough time for the plaque to calcify). In general, a coronary calcium score of zero is a good prognostic sign. How long does that prognostic value last? What is the warranty period of a calcium score of zero? A study showed that about 15% of people with initial calcium score of zero progressed to a score over 10 in about 5 to 8 years. In the study it was rare to progress to a calcium score over 100. Diabetic patients, active smokers and those with strong family history progressed more quickly. Based on these data, it is recommended that statin therapy be withheld for a patient with a calcium score of zero, unless they have diabetes, are smoking or there is a family history of premature heart disease. How often should the calcium score be repeated to reassess risk? For patients with a coronary calcium score of zero, repeating the study is recommended in 3 to 5 years. For patients with an elevated coronary calcium score who are already on statin, it is not recommended to have a follow up study. The reason is that the calcium score may go up on statin treatment. If the score goes up, we don’t know if there has been further plaque progression or increasing calcium in existing plaque- a sign of healing.

 

Using the coronary calcium can help predict the risk for future heart events in patients between 40 and 75 years old who have not yet had a cardiac issue (primary prevention). If you are like Bill and your coronary calcium score is greater than zero, initiating lifestyle changes and starting a statin can reduce the risk for a heart event in the future. If you are lucky like Hillary and your coronary calcium score is zero, the risk for future events is low. However, it is not a “get out jail free” card nor are you “saved by zero”. If coronary calcium score is zero and LDL cholesterol is high, then lifestyle changes should be incorporated even if starting a statin may be avoided. Vigilance is necessary with follow up lipid panels and repeat coronary calcium testing in 3 to 5 years. 

POTS or Why Am I Dizzy When I Stand Up?

 

When you think about, we shouldn’t be able to stand upright. Our ancient ancestors, floating around in the sea, used the water for everything; hydration, nutrition and support. The water buoyed them, there was no need for a spine or other elaborate bony structures. To leave the water and especially to walk upright on two legs, certain adaptations were needed. Skeletal features that evolved over time included a spine, hip bones, thigh bones and the muscles needed to keep the body upright and erect. Circulatory adaptations were needed as well. When we are upright, the heart has to pump blood against gravity to keep blood flowing to the brain. Blood pressure to the brain must be maintained otherwise when we stand up, the blood pressure would drop, the blood flow to the brain would decrease and we would pass out. How does the circulation respond to standing and why don’t we routinely pass out?

 

The mechanism that evolved to keep us upright is a blood pressure feedback loop that involves the heart, the brain and the blood vessels. On standing, blood pools in the veins in the legs. This causes a transient decrease in blood pressure. This drop in blood pressure is recognized by a sensor in the carotid artery (the carotid artery is the main artery supplying blood to the brain, the sensor is located in the carotid sinus, just outside of the skull). When the carotid sinus senses a lower blood pressure, it fires nerves which activate the sympathetic system. The sympathetic system constricts blood vessels, increases the heart rate and increases the amount of blood pumped by the heart ultimately restoring normal blood pressure to the brain and preventing passing out.

 

This mechanism is very effective at maintaining blood pressure. However, there are circumstances where the mechanism is overwhelmed causing dizziness or passing out. Instances include prolonged standing in a hot environment (think of a soldier standing for a long time in the hot sun), dehydration, or deconditioning from staying in bed for a long time. As we age, the mechanism isn’t as fast and we can have dizziness on rising quickly from a sitting or lying down position. If the mechanism isn’t working, it leads to passing out on standing, a condition called orthostatic hypotension (from the Greek ortho- straight and statikos- causing to stand; caused by standing erect; hypotension- low blood pressure). Orthostatic hypotension is defined as a drop in systolic blood pressure of 20 mmHg or more within three minutes of standing. It is a significant medical problem whose incidence rises after age 65. It occurs in 6% of elderly people in the community and up to 50% of people in nursing homes. Orthostatic hypotension puts patients at risk for falls, as well as cardiac disease. Orthostatic hypotension occurs in patients with degenerative diseases of the autonomic nervous system (for example, Parkinson’s disease). It also occurs due to an impaired autonomic nervous system (for example, diabetes). Orthostatic hypotension can be diagnosed in the office or at the hospital bedside by checking blood pressure lying down and standing up. The formal way to diagnose it is with a tilt table test (strapping a patient to an upright table and checking blood pressure frequently). 

 

There are multiple ways to treat orthostatic hypotension. In milder forms, patients recognize that they are about to pass out and can sit or lay down to avoid falling. For more significant cases, the first step is to stop medications that can lower the blood pressure or exaggerate orthostatic symptoms. Medications to avoid include diuretics, most blood pressure meds, prostate medications (ex, Flomax or tamsulosin), antiparkinson agents and antidepressants. Other measures include increasing blood volume by keeping hydrated, ingesting salt tablets, or using a medication (fludrocortisone) which promotes salt retention. Pooling of blood in the veins of the lower legs can be decreased by using compression stockings. Lastly, medications that stimulate the sympathetic nervous system (such as midodrine or droxidopa, Northera) can be used. 

 

POTS (postural orthostatic tachycardia syndrome) is the most common form of orthostatic intolerance in young people. It usual affects young, pre-menopausal women with as many as 500,000 cases in the US. It is defined as an increase in the heart rate of 30 beats per minute or more within 10 minutes of standing, but without a decrease in blood pressure. The typical patient is a 30-year-old woman with a heart rate increment of 40 beats per min or more. Cardiovascular deconditioning is common. Therefore, the key to treatment is exercise. The exercise regimen should avoid the upright position (swimming or recumbent bike can be prescribed) until fitness improves. Liberal intake of fluids and salt, compression stockings and sleeping with the head of the bed greater than 30 degrees are other methods. Medications can be used in severe cases and include the same agents used for orthostatic hypotension. 

 

Whether you are young or old, if you have dizziness on rising there are measures you can take to avoid symptoms. If you have more severe symptoms or are passing out on standing, see your doctor to work through how to keep yourself upright. 

How Sweet It Is!

 

Ralph: (growling) Where's my morning coffee?

Alice: Here you go Ralph

Ralph: (sipping) That tastes terrible!

Alice: We ran out of sugar

Ralph: One of these days, Alice. One of these days. 

Alice: Try this new artificial sweetener

Ralph (sipping) How sweet it is!

 

If you are of a certain age, you can identify these characters from the 1950’s television show "The Honeymooners" and you’ll recognize the Ralph Kramden/Jackie Gleason catchphrase, "How sweet it is!". So how sweet are artificial sweeteners? Depending on the agent, artificial sweeteners are 200 to 600 times sweeter than sugar. However, are they healthier than sugar? Are there any heart issues with artificial sweeteners?

 

Sugar seems to be the new bad guy on the block, not without reason. Everyone likes a sugary snack every now and then, but can it be limited to just one snack? Sugar triggers a reaction in our brain and makes us crave more. Sugar begets sugar. So, instead of stopping at one serving, more sugar is desired and before you know it, the whole candy bar is gone. All that sugar consumption adds empty calories, resulting in obesity, diabetes and heart disease. Even natural sweeteners, such as honey or molasses are a form of added sugar and add calories to the diet. To counteract the health effects of sugar, artificial sweeteners were developed and have been available for decades. Artificial sweeteners taste sweet like sugar but have no or few calories. They allow people to enjoy the sweetness of foods and drinks but without excess calories.  In this way, artificial sweeteners can help with weight loss. US and European health agencies have deemed artificial sweeteners safe in limited amounts and extensive research has not shown a higher risk of cancer. It had been felt that these sugar substitutes do not cause serious health problems. Until now.

 

Recent research on artificially sweetened beverages has shown a link to heart disease. A French study started in 2009 and including 104,000 participants found that people who drank 6 ounces or more per day of artificially sweetened beverages had a higher risk for cardiovascular disease. Artificial sweetened beverages included drinks that contained aspartame (also used in NutraSweet, Equal) and sucralose (found in Splenda). Another study of 9000 participants followed for 10 years showed that those who drank greater than two liters per week (about 10 ounces per day) of an artificially sweetened beverage had an increased risk for atrial fibrillation. One last study followed 2,888 participants and found artificially sweetened drinks to be associated with a higher risk of stroke and dementia. So, these beverages may not be a healthy substitute for sugary soft drinks.

 

The data on two artificial sweeteners, both from the sugar alcohol category, seems especially troubling. Erythritol is a no calorie sugar substitute used in many products including protein bars, yogurt, cookies and ice cream. It occurs naturally in melons and grapes. It is also the primary sweetener in the low carbohydrate high fat keto diet. A 2023 study of 1100 people found that high levels of erythritol in the blood was associated with an increased risk of heart attack, stroke and death. A more recent study may explain why. Twenty healthy volunteers were given drinks sweetened with a typical amount of erythritol or a drink with sugar. When given erythritol, the blood platelets were activated putting people at risk for blood clotting, heart attack or stroke. The same platelet effect was not seen when consuming a sugar drink. Another sugar alcohol artificial sweetener, xylitol, has similar data. Xylitol is found naturally in fruit and vegetables. It is also used to sweeten gum and toothpaste. In a study of 3000 people in the US and Europe, those with the highest level of xylitol in the blood were more likely to have heart or blood vessel problems. Another study followed 1100 people for three years. Xylitol was associated with major adverse cardiac events and was shown to activate platelets, similar to erythritol. 

 

As daunting as this data is, experts have not declared any artificial sweetener a cardiac risk. However, more and better research is needed on these agents, especially the potential cardiovascular effects. Before you declare “How sweet it is!” and consume artificial sweeteners with impunity, keep an eye out for future research on the safety of these agents. For now, using them in small, limited quantities seems to be safe. 

 

The Siesta

The Siesta (or La Meridienne in French) is a famous painting by the artist Vincent Van Gogh. It depicts a siesta and symbolizes life in rural France in the late 1880’s. Siesta is a Spanish word meaning a short nap, usually taken in the afternoon, after lunch. In warm weather climates workers who do physical labor need to take a break to avoid the hottest part of the day. Siestas are common in Mediterranean countries, the Middle East, China, Latin America and the Philippines. Siestas are both practical and cultural. There are studies from Greece showing that naps are associated with a lower risk for heart attack. What is the data on siestas? How does day time napping affect cardiac health?

 

The health data on siestas is quite variable, showing some good and some bad effects. In a study from 2019, taking a daytime nap was associated with lower blood pressure. In those that nap, the blood pressure was 5 mmHg lower than in those that didn’t nap. Usually when something lowers blood pressure there is concomitant lowering of cardiac risk.  That doesn’t seem to be the case with napping. A comprehensive review of relevant studies showed that daytime napping over 60 minutes was associated with an increased risk for cardiac disease and mortality.  Another study followed 116, 000 people for 8 years and found that napping was associated with increased for major cardiac events and death in those that slept on average more than six hours per night. No increased risk was found in people who slept less than 6 hours per night. It was felt that naps compensated for lack of sleep for people who didn’t get enough sleep at night. The most recent study found some disturbing trends. The trial studied 476,000 people determining that 56% never or rarely took a nap, 38% sometimes napped and 5% usually took a daytime nap. Compared to people who never or rarely napped, frequent daytime napping increased the risk for atrial fibrillation and for dementia. This is the first time this association was made regarding the siesta. Why does napping lead to atrial fibrillation? One hypothesis is that napping indicates inadequate nighttime sleep from undiagnosed sleep apnea, a condition well known to cause atrial fibrillation. In addition, atrial fibrillation is a risk for dementia. 

 

It appears that frequent daytime napping can lead to dementia. What is the optimal amount of sleep to avoid dementia? The largest sleep study ever conducted just finished and concluded that 7 hours of sleep per night was the right amount for reasoning, verbal skills and overall cognitive thinking.  Sleeping more or less than that could lead to cognitive decline and dementia. What other new data has emerged regarding dementia? Eating processed red meat and sugar have been associated with dementia. Processed red meat (including bacon, hot dogs, sausages, salami, cold cuts) has been tied to an increased risk of cancer, heart disease and diabetes. A new study that tracked 100,000 people over four decades showed that eating two servings of red meat each week increased the risk for dementia by 14% and was associated with worse memory and thinking skills. The study also showed that replacing red meat with nuts, beans or tofu lowered the risk for cognitive decline by 23%. Processed red meat may affect the brain because of harmful chemicals such as nitrites and the increased sodium content can lead to high blood pressure. The study only found an association but did not prove cause and effect. So, we don’t know if red meat itself causes dementia or if people who avoid red meat are generally more health conscious. Unprocessed red meat, such as ground beef or steak, was not linked to dementia in the trial. In other news, on World Brain Day (July 22 2024), the German Society of Neurology warned that too much sugar can harm the brain.  High blood sugar levels can damage blood vessels, causing plaque, decreasing blood flow and causing vascular dementia. In addition, sugar directly affects the nerve cells, impairing cognition. What should be eaten instead? Try to eat whole fresh foods (fruits, vegetables, fish, nuts, beans) and the less processed, the better. Whole fresh foods bring protein, fiber, nutrients, minerals and vitamins the brain promoting a healthier body and longer lifespan.

 

Last month we found out that to decrease your risk for dementia you should take your blood pressure medications, go to the shore, plop down on a beach chair and watch the waves roll in. This month we learn that, to further lower your risk for dementia, try not to nap in that beach chair. In addition, skip the hot dog, ice cream and cotton candy on the boardwalk. It is hard to do, but it may be well worth it. 

Beach Blanket Blood Pressure

 

It’s July! Summer time! Time to vacation and unwind. Head to your favorite beach, plop down on your beach chair and watch the waves role in. You can feel yourself relaxing, calming down. You can actually feel your blood pressure (BP) dropping. Does the presence of water really lower BP? Researchers actually did this study. They found that viewing water in an outdoor setting (for example a lake) reliably lowered BP compared to looking at grass field. Aside from water watching, what else is new in the world of hypertension (high blood pressure)?

 

Before diving into new data, some basics about hypertension. Despite knowing about high BP for more than 100 years and despite the fact that nearly 50% of the population has hypertension, we still do not know what causes it. What is the definition of hypertension? Hypertension is diagnosed as a BP greater than 130/80 on multiple occasions over several weeks. What is the ideal BP? 115/75. Several studies have shown that treating BP to under 120 mmHg improved outcomes versus treating to a BP under 140 mmHg. The under 120 mmHg group had fewer heart events, lower mortality and less cognitive decline. It is important to understand that the BP is not one single, stable number. Rather BP goes up and down, like waves on the ocean, with activity, time of day, and medications among other factors. The goal is to have nice, calm undulating waves of BP, not tidal waves with extreme highs and very low lows. Also, the goal is to have the BP average under 140 mmHg, or more ideally, under 120 mmHg. Hypertension is treated with lifestyle modifications and medications. Lifestyle changes include exercise, weight loss, smoking cessation and following a DASH diet. Sodium reduction (a low salt diet) is also important for treatment. First line medications for hypertension fall into three classes of drugs: diuretics (hydrocholorothiazide, chlorthalidone), calcium channel blockers (amlodipine) and angiotension converting enzyme inhibitors (lisinopril, ramipril) or angiotension receptor blockers (losartan, olmesartan). Reducing BP with medications reduces the risk of dying, reduces stroke by 35-40%, reduces heart attack by 20-25%, reduces heart failure by more than 50% and decreases the risk for dementia and cognitive impairment. 

 

Of the three classes of medications, which one is best? A recent study followed 33,000 patients for 23 years looking at the three types of medications and assessing outcomes. The researchers found no difference among the three classes in their BP lowering efficacy and no difference in cardiovascular mortality or stroke. 

 

In this era of BP medications is a low salt diet still recommended? High sodium (salt) intake has long been associated with hypertension. BP clearly goes up with sodium intake of 2 grams per day (2 grams of sodium is about 88% of a teaspoon of table salt). It is estimated that Americans eat on average 3.4 grams of salt per day. The optimal goal for salt intake is about 1.5 grams per day. Lowering sodium intake can reduce BP by 5 to 6 mmHg. Does this effect persist if patients are already on BP meds? A recent trial studied 213 people on BP medications. They were given a high sodium diet for one week, then a low sodium diet the second week and their BPs were tracked. BP was 8 mmHg higher on the high sodium diet. The low sodium diet consistently lowered BP, on top of the presence of medication. The conclusion, “Don’t underestimate the power of salt”.

 

Elevated systolic BP is linked to mild cognitive impairment and dementia. Hypertension may cause dementia by direct and indirect methods. A direct mechanism is the known risk between hypertension and stroke. Multiple small strokes due to elevated BP can cause dementia over time. An indirect mechanism is atrial fibrillation. Hypertension is associated with atrial fibrillation, which in turn can cause blood clots which break off from the heart and travel to the brain. It has long been felt, but not proven, that BP lowering reduced the risk for dementia. However, new data is beginning to emerge. Now we have learned that just by taking medication, dementia can be avoided. A study from Italy followed 215,000 patients for seven years. The patients were starting BP medications for the first time. It was found that the patients who were more adherent to their BP meds (more likely to take their meds) had lower odds of going on to dementia. Another recent study was the first definitive trial to show that BP reduction lowered the risk for dementia. The study looked at 34,000 patients age 40 and older. In patients with intensive BP reduction (goal < 130/80), dementia was lowered by 15% and cognitive impairment improved as well. These results are exciting because now there is a potential tool to prevent dementia. 

 

In order to control your blood pressure and reduce your risk for dementia this summer, don’t forget to take your medications regularly, follow a low salt diet and head out to the beach.